title: Factor v Leiden and antiphospholipid antibodies in either mothers or infants increase the risk for perinatal arterial ischemic stroke.
abstract: OBJECTIVE
  The objective was to investigate the role of infant and maternal thrombophilia in a cohort of mothers and infants presenting with perinatal arterial ischemic stroke.
  
  
  METHODS
  Forty-seven infants with clinically and radiologically confirmed perinatal arterial ischemic stroke underwent thrombophilia workup: factor V Leiden (FVL), PII20210A mutation, Methylene-tetrahydrofolate reductase 677T polymorphism, protein C, protein S, antithrombin, FVIII, and antiphospholipid antibodies. Thrombophilia data were available for 23 mother-infant pairs and compared with control populations to evaluate the risk for PAS.
  
  
  RESULTS
  Thirty of 47 (64%) infants and 15 of 22 mothers (68%) had evidence of thrombophilia. In 18 of 23 (78%) mother-infant pairs, there was at least 1 thrombophilic risk factor, but 15 pairs were mismatched in pathology. Among infants, FVL, protein C deficiency, and presence of antiphospholipid antibodies prevailed (OR, 4.2; 95% CI, 1.5-11.3; OR, 12.2; 95% CI, 2.5-59.9; OR, 4.1; 95% CI, 1.4-12.2, respectively). Interestingly FVL prevailed in almost one-third of mothers (OR, 8.5; 95% CI, 4.1-17.5) and 18% of mothers had antiphospholipid antibodies (OR, 3.8l; 95% CI, 1.5-10.0).
  
  
  CONCLUSIONS
  Maternal and neonatal thrombophilia, especially presence of FVL or antiphospholipid antibodies, may be important in the pathogenesis of perinatal arterial ischemic stroke. The nature of thrombophilic mother-infant risk potential interactions warrants further investigation.
authors.affiliation: Thrombosis Unit, National Hemophilia Center, Sheba Medical Center, Tel-Hashomer, Israel. gili.kenet@sheba.health.gov.il
authors.forename: Michal J
authors.initials: MJ
authors.lastname: Simchen
authors.forename: Gal
authors.initials: G
authors.lastname: Goldstein
authors.forename: Aaron
authors.initials: A
authors.lastname: Lubetsky
authors.forename: Tzipi
authors.initials: T
authors.lastname: Strauss
authors.forename: Eyal
authors.initials: E
authors.lastname: Schiff
authors.forename: Gili
authors.initials: G
authors.lastname: Kenet
mesh_terms: D000293:Adolescent; D001323:Autoantibodies / Q000032:analysis / Q000097:blood*; D015415:Biomarkers / Q000032:analysis; D002545:Brain Ischemia / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D005165:Factor V / Q000235:genetics*; D005260:Female; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008431:Maternal-Fetal Exchange / Q000235:genetics / Q000276:immunology; D009154:Mutation / Q000235:genetics; D010743:Phospholipids / Q000276:immunology*; D011247:Pregnancy; D011446:Prospective Studies; D012307:Risk Factors; D020521:Stroke / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D019851:Thrombophilia / Q000235:genetics* / Q000276:immunology / Q000473:pathology
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D005819:Genetic Markers; D010743:Phospholipids; C095381:factor V Leiden; D005165:Factor V